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G Camussi - One of the best experts on this subject based on the ideXlab platform.
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human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
The FASEB Journal, 2007Co-Authors: Maria M Zanone, Mark Peakman, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Nigel Klein, Paolo Cavallo Perin, Pier G Conaldi, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1β and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-α. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfect...
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Human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection.
FASEB J, 2007Co-Authors: G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1Beta and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-alpha. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfected monolayers. Moreover, infection up-regulated the viral receptors HCAR and DAF and coreceptor alpha(v)Beta3 integrin on islet MECs, while down-regulating expression of HCAR on human aortic endothelial cells, indicating potential tissue-specific influence on the pathological outcome of infection. These results provide evidence that islet MECs are natural targets and reservoirs for persistent CVB infection resulting in acute endothelial cell activation By Virus, which may contriBute to selective recruitment of suBsets of leukocytes during inflammatory immune responses, such as insulitis in type 1 diaBetes.
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Human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
'FASEB', 2007Co-Authors: Maria M Zanone, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Pier G Conaldi, N.j. Klein, Cavallo P. Perin, M. Peakman, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1 f and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfected monolayers. Moreover, infection up-regulated the viral receptors HCAR and DAF and coreceptor v f3 integrin on islet MECs, while down-regulating expression of HCAR on human aortic endothelial cells, indicating potential tissue-specific influence on the pathological outcome of infection. These results provide evidence that islet MECs are natural targets and reservoirs for persistent CVB infection resulting in acute endothelial cell activation By Virus, which may contriBute to selective recruitment of suBsets of leukocytes during inflammatory immune responses, such as insulitis in type 1 diaBetes
Gun Frisk - One of the best experts on this subject based on the ideXlab platform.
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antiviral treatment of <B>CoxsackieB> B Virus infection in human pancreatic islets
Antiviral Research, 2007Co-Authors: Annakarin Berg, Annika Olsson, Olle Korsgren, Gun FriskAbstract:EnteroVirus infections of the pancreatic islets are Believed to trigger or precipitate the near total destruction of Beta-cells that constitutes type 1 diaBetes (T1D). This study investigated the aBility of an anti-picornaviral compound, pleconaril, to Block the replication of two Beta-cell tropic <B>CoxsackieB> B4 Virus (CBV-4) strains in isolated human islets. The two strains, VD2921 and V89 4557, with demonstrated aBilities to cause non-lytic persistence or lytic infection, respectively, in islets, represented two different potential mechanisms Behind Virus-induced T1D. The Virus replication in the islets was studied with and without addition of pleconaril. In addition, islet morphology was studied every day. To test the effects of pleconaril and/or DMSO on the Beta-cells' insulin secretion, glucose perifusions were performed on treated and untreated islets. Virus titrations showed a clear reduction of the replication of Both strains after pleconaril treatment. The VD2921 strain was inhiBited to undetectaBle levels. The V89 4557 strain, however, showed an initial reduction of titers But Virus titers then increased despite the addition of a second dose of pleconaril. This incomplete inhiBition of viral replication suggested the existence of a resistant suBtype within this strain. Pleconaril treatment reduced the Beta-cells' insulin secretion in response to glucose stimulation in some experiments and induced slight morphological changes to the islets compared to untreated controls. In summary, pleconaril reduced the replication of the two Beta-cell tropic CBV-4 strains in human islets. However, genetic differences Between these strains influenced the effectiveness of pleconaril treatment. This stresses the importance of using multiple viral strains in antiviral tests.
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the replication of certain <B>CoxsackieB> B Virus strains in cho cells
Journal of Virological Methods, 2001Co-Authors: Gun Frisk, Thomas Elfstrom, Hans DiderholmAbstract:Cell surface molecules that can act as viral receptors may exert an important selective pressure on RNA viral quasi-species. <B>CoxsackieB>-AdenoVirus Receptor and Decay Accelerating Factor (DAF, CD55) have Been identified as receptors for <B>CoxsackieB> B Virus. In studies of viral replication using different strains of <B>CoxsackieB>Virus serotype 4 (CBV-4), it was found that despite lack of expression of these cell surface molecules on Chinese Hamster Ovary (CHO) cells and despite their common use as negative controls in <B>CoxsackieB> B Virus receptor assays, two strains were aBle to replicate, one (V89-4557) without cytopathic effect (CPE), and the other (T318) with strong CPE. A weak signal was oBtained using antiBodies against enteroVirus, visualized with FITC-conjugated antiBodies, when the <B>CoxsackieB>Virus B4 strain V89-4557 was inoculated on CHO cells compared to no signal with the non-replicating <B>CoxsackieB>Virus B4 strain VD2921, indicating some degree of Binding of the former to the cells.
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indications that maternal <B>CoxsackieB> B Virus infection during pregnancy is a risk factor for childhood onset iddm
Diabetologia, 1995Co-Authors: Gisela Dahlquist, Gun Frisk, S A Ivarsson, L Svanberg, Marianne Forsgren, Hans DiderholmAbstract:In a population-Based setting, we traced serum samples collected at time of Birth from 55 mothers whose children later developed insulin-dependent diaBetes (IDDM) and matched them pairwise to control suBjects who gave Birth at the same hospital during the same month. The sera were analysed for IgM antiBodies to <B>CoxsackieB> B Virus serotypes 2, 3 and 4 (CBV-2, 3 and 4) using a type-specific Μ-antiBody-capture radioimmunoassay. Despite a decreased power due to the close matching By time of Birth we found a significantly higher frequency of CBV-3 IgM at delivery in mothers whose children later Became diaBetic compared to their matched control suBjects. When using the presence of CBV-3 IgM as a risk factor the Mantel-Haenszel odds ratio estimate (95% confidence limits) was 2.57 (1.02; 7.31), p=0.043. For CBV-2 and CBV-4, respectively no significant difference was found Between mothers of patients and control suBjects. According to the odds ratio estimate for CBV-3 and the proportion of exposed mothers among patients estimated in this study the aetiological fraction for this risk determinant would Be 27%. In conclusion, this study indicates that children of mothers who expressed CBV IgM at delivery are at increased risk for developing childhood onset IDDM. A fetal infection with CBV similar to ruBella Virus may initiate autoimmunity or cause persistent infection that may lead to progressive Beta-cell destruction.
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<B>CoxsackieB> B Virus infections in women with miscarriage
Journal of Medical Virology, 1993Co-Authors: C Axelsson, Gun Frisk, K Bondestam, S Bergstrom, Hans DiderholmAbstract:To study the possiBle role of <B>CoxsackieB> B Virus serotypes 1-5 (CBV 1-5) as an etiological factor in miscarriage, 97 women with miscarriage were tested for the presence of CBV-IgM By radioimmunoassays (RIAs) and compared with 113 control women undergoing voluntary interruption of pregnancy in the same gestational week. Of the 80 women with miscarriage Before the 13th week of gestation, 34 (42%) had CBV-IgM, whereas 18 of 100 (18%) corresponding control women had these antiBodies, a statistically significant difference (P < 0.001). There was no significant difference in CBV-IgM frequency Between the women with miscarriage from the 13th through the 27th week and their controls. IgM against CBV 2 predominated, followed By IgM against CBV 5, CBV 4, CBV 3, and CBV 1. Two strains of CBV 5 were used in the RIAs, one (M147) isolated from a woman with miscarriage included in the study and one (V136) isolated in 1971 from a patient with meningitis. When the former strain was used, 13 women with miscarriage and seven control women had IgM, But with use of V136 only two women in each group were IgM positive. CBV 5 was isolated from the placental tissue from more women with miscarriage (6 of 28; 21%), than control women (2 of 21; 10%), But the difference was not statistically significant. No other Viruses, except cytomegaloVirus from a woman with miscarriage, were isolated.
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increased frequency of <B>CoxsackieB> B Virus igm in women with spontaneous aBortion
Journal of Infection, 1992Co-Authors: Gun Frisk, Hans DiderholmAbstract:Summary IgM antiBodies to <B>CoxsackieB> B Virus serotypes 1–5 (CBV 1–5) were studied By radioimmunoassay (RIA) of Blood samples from women who had undergone a spontaneous aBortion or given Birth to a stillBorn child. Results were compared with those of controls comprising healthy pregnant women who had not suffered such experiences. Among 48 women with aBortions, 16 (33 %) had CBV-IgM, while among the controls only three of 37 (8 %) had these antiBodies, a statistically significant difference ( P
Hans Diderholm - One of the best experts on this subject based on the ideXlab platform.
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the replication of certain <B>CoxsackieB> B Virus strains in cho cells
Journal of Virological Methods, 2001Co-Authors: Gun Frisk, Thomas Elfstrom, Hans DiderholmAbstract:Cell surface molecules that can act as viral receptors may exert an important selective pressure on RNA viral quasi-species. <B>CoxsackieB>-AdenoVirus Receptor and Decay Accelerating Factor (DAF, CD55) have Been identified as receptors for <B>CoxsackieB> B Virus. In studies of viral replication using different strains of <B>CoxsackieB>Virus serotype 4 (CBV-4), it was found that despite lack of expression of these cell surface molecules on Chinese Hamster Ovary (CHO) cells and despite their common use as negative controls in <B>CoxsackieB> B Virus receptor assays, two strains were aBle to replicate, one (V89-4557) without cytopathic effect (CPE), and the other (T318) with strong CPE. A weak signal was oBtained using antiBodies against enteroVirus, visualized with FITC-conjugated antiBodies, when the <B>CoxsackieB>Virus B4 strain V89-4557 was inoculated on CHO cells compared to no signal with the non-replicating <B>CoxsackieB>Virus B4 strain VD2921, indicating some degree of Binding of the former to the cells.
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indications that maternal <B>CoxsackieB> B Virus infection during pregnancy is a risk factor for childhood onset iddm
Diabetologia, 1995Co-Authors: Gisela Dahlquist, Gun Frisk, S A Ivarsson, L Svanberg, Marianne Forsgren, Hans DiderholmAbstract:In a population-Based setting, we traced serum samples collected at time of Birth from 55 mothers whose children later developed insulin-dependent diaBetes (IDDM) and matched them pairwise to control suBjects who gave Birth at the same hospital during the same month. The sera were analysed for IgM antiBodies to <B>CoxsackieB> B Virus serotypes 2, 3 and 4 (CBV-2, 3 and 4) using a type-specific Μ-antiBody-capture radioimmunoassay. Despite a decreased power due to the close matching By time of Birth we found a significantly higher frequency of CBV-3 IgM at delivery in mothers whose children later Became diaBetic compared to their matched control suBjects. When using the presence of CBV-3 IgM as a risk factor the Mantel-Haenszel odds ratio estimate (95% confidence limits) was 2.57 (1.02; 7.31), p=0.043. For CBV-2 and CBV-4, respectively no significant difference was found Between mothers of patients and control suBjects. According to the odds ratio estimate for CBV-3 and the proportion of exposed mothers among patients estimated in this study the aetiological fraction for this risk determinant would Be 27%. In conclusion, this study indicates that children of mothers who expressed CBV IgM at delivery are at increased risk for developing childhood onset IDDM. A fetal infection with CBV similar to ruBella Virus may initiate autoimmunity or cause persistent infection that may lead to progressive Beta-cell destruction.
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<B>CoxsackieB> B Virus infections in women with miscarriage
Journal of Medical Virology, 1993Co-Authors: C Axelsson, Gun Frisk, K Bondestam, S Bergstrom, Hans DiderholmAbstract:To study the possiBle role of <B>CoxsackieB> B Virus serotypes 1-5 (CBV 1-5) as an etiological factor in miscarriage, 97 women with miscarriage were tested for the presence of CBV-IgM By radioimmunoassays (RIAs) and compared with 113 control women undergoing voluntary interruption of pregnancy in the same gestational week. Of the 80 women with miscarriage Before the 13th week of gestation, 34 (42%) had CBV-IgM, whereas 18 of 100 (18%) corresponding control women had these antiBodies, a statistically significant difference (P < 0.001). There was no significant difference in CBV-IgM frequency Between the women with miscarriage from the 13th through the 27th week and their controls. IgM against CBV 2 predominated, followed By IgM against CBV 5, CBV 4, CBV 3, and CBV 1. Two strains of CBV 5 were used in the RIAs, one (M147) isolated from a woman with miscarriage included in the study and one (V136) isolated in 1971 from a patient with meningitis. When the former strain was used, 13 women with miscarriage and seven control women had IgM, But with use of V136 only two women in each group were IgM positive. CBV 5 was isolated from the placental tissue from more women with miscarriage (6 of 28; 21%), than control women (2 of 21; 10%), But the difference was not statistically significant. No other Viruses, except cytomegaloVirus from a woman with miscarriage, were isolated.
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increased frequency of <B>CoxsackieB> B Virus igm in women with spontaneous aBortion
Journal of Infection, 1992Co-Authors: Gun Frisk, Hans DiderholmAbstract:Summary IgM antiBodies to <B>CoxsackieB> B Virus serotypes 1–5 (CBV 1–5) were studied By radioimmunoassay (RIA) of Blood samples from women who had undergone a spontaneous aBortion or given Birth to a stillBorn child. Results were compared with those of controls comprising healthy pregnant women who had not suffered such experiences. Among 48 women with aBortions, 16 (33 %) had CBV-IgM, while among the controls only three of 37 (8 %) had these antiBodies, a statistically significant difference ( P
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<B>CoxsackieB> B Virus igm in children at onset of type 1 insulin dependent diaBetes mellitus evidence for igm induction By a recent or current infection
Diabetologia, 1992Co-Authors: Gun Frisk, Goran Friman, Jan Fohlman, Torsten Tuvemo, Hans DiderholmAbstract:Thirty-five children with newly-diagnosed Type 1 (insulin-dependent) diaBetes mellitus and their 47 siBlings were investigated for the presence of IgM antiBodies to <B>CoxsackieB> B Virus serotypes 1-5 (CBV 1-5) with the aid of mu-antiBody-capture radioimmunoassays. When a high cut-off value was used, 16 (46%) diaBetic children and 16 (34%) siBlings showed CBV-IgM. Of the siBlings of diaBetic patients positive for CBV-IgM, 11 (44%) were CBV-IgM-positive; the corresponding figure for the siBlings of negative patients was five (26%). With a lower cut-off value, leading to a "Borderline titre", the frequency of IgM positivity increased in Both the patients and siBlings. When the Borderline titres were included, the numBer of IgM-positive patients was 19 (54%) and the corresponding numBer of siBlings was 29 (62%). Of the siBlings of positive patients, 27 (93%) showed CBV-IgM, and of the siBlings of the negative patients, two (11%) were CBV-IgM-positive. Sixteen (89%) siBlings of IgM-negative patients remained negative. Regarding the serotypes of CBV to which IgM was directed, CBV 4 was most frequent, followed By serotypes CBV 3, CBV 2, CBV 5 and CBV 1. There was a striking similarity Between the individual diaBetic child and his or her siBling(s) concerning this specificity of IgM. It is concluded that within most families with a newly-diagnosed diaBetic child positive for CBV-IgM the same serotype(s) of the Virus circulates and that the intrafamilial spread of Virus is consideraBle. The results strongly indicate that the IgM detected was CBV-specific and caused By a recent or current CBV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
Maria M Zanone - One of the best experts on this subject based on the ideXlab platform.
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human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
The FASEB Journal, 2007Co-Authors: Maria M Zanone, Mark Peakman, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Nigel Klein, Paolo Cavallo Perin, Pier G Conaldi, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1β and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-α. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfect...
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Human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
'FASEB', 2007Co-Authors: Maria M Zanone, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Pier G Conaldi, N.j. Klein, Cavallo P. Perin, M. Peakman, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1 f and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfected monolayers. Moreover, infection up-regulated the viral receptors HCAR and DAF and coreceptor v f3 integrin on islet MECs, while down-regulating expression of HCAR on human aortic endothelial cells, indicating potential tissue-specific influence on the pathological outcome of infection. These results provide evidence that islet MECs are natural targets and reservoirs for persistent CVB infection resulting in acute endothelial cell activation By Virus, which may contriBute to selective recruitment of suBsets of leukocytes during inflammatory immune responses, such as insulitis in type 1 diaBetes
Pier G Conaldi - One of the best experts on this subject based on the ideXlab platform.
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human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
The FASEB Journal, 2007Co-Authors: Maria M Zanone, Mark Peakman, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Nigel Klein, Paolo Cavallo Perin, Pier G Conaldi, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1β and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-α. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfect...
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Human pancreatic islet endothelial cells express <B>CoxsackieB>Virus and adenoVirus receptor and are activated By <B>CoxsackieB> B Virus infection
'FASEB', 2007Co-Authors: Maria M Zanone, Enrica Favaro, Elena Ferioli, Guo Cai Huang, Pier G Conaldi, N.j. Klein, Cavallo P. Perin, M. Peakman, G CamussiAbstract:EnteroViruses, such as the <B>CoxsackieB>Virus (CV) group, have Been linked to the induction of inflammatory and autoimmune diseases. Virus tropism and tissue access are modulated By endothelial cells. To examine the susceptiBility of microvascular endothelial cells (MECs) derived from pancreatic islets to infection with CV group B (CVB), purified cultured human islet MECs were infected with CVB-4 strain, and the immunological phenotype of the infected cells was analyzed. CVB-4 persistently infected the islet MECs, which expressed the CV receptors human <B>CoxsackieB>Virus and adenoVirus receptor (HCAR) and decay accelerating factor (DAF) and maintained EC characteristics, without overt cytopathic effects. CVB-4 infection transiently up-regulated expression of the adhesion molecules ICAM-1 and VCAM-1 and increased production of the proinflammatory cytokines IL-1 f and IL-6, and chemokines IL-8 and lymphotactin, as well as IFN-. Mononuclear cell adhesion to CVB infected monolayers was increased, compared to uninfected monolayers. Moreover, infection up-regulated the viral receptors HCAR and DAF and coreceptor v f3 integrin on islet MECs, while down-regulating expression of HCAR on human aortic endothelial cells, indicating potential tissue-specific influence on the pathological outcome of infection. These results provide evidence that islet MECs are natural targets and reservoirs for persistent CVB infection resulting in acute endothelial cell activation By Virus, which may contriBute to selective recruitment of suBsets of leukocytes during inflammatory immune responses, such as insulitis in type 1 diaBetes
